Atherogenic stimuli, including dyslipidemia, hypertension, and smoking, lead to endothelial dysfunction and structural alterations to the arterial walls and trigger the accumulation of circulating apolipoprotein B (apoB)-containing lipoproteins, mainly low-density lipoproteins (LDLs), in the intima region of the arterial wall [21,22]. This evidence concerns the gene APOB and metabolic syndrome.